A water-damaged home and health of occupants: a case study.

A family of five and pet dog who rented a water-damaged home and developed multiple health problems. The home was analyzed for species of mold and bacteria. The diagnostics included MRI for chronic sinusitis with ENT and sinus surgery, and neurological testing for neurocognitive deficits. Bulk samples from the home, tissue from the sinuses, urine, nasal secretions, placenta, umbilical cord, and breast milk were tested for the presence of trichothecenes, aflatoxins, and Ochratoxin A. The family had the following diagnosed conditions: chronic sinusitis, neurological deficits, coughing with wheeze, nose bleeds, and fatigue among other symptoms. An infant was born with a total body flare, developed multiple Cafe-au-Lait pigmented skin spots and diagnoses with NF1 at age 2. The mycotoxins were detected in bulk samples, urine and nasal secretions, breast milk, placenta, and umbilical cord. Pseudomonas aueroginosa, Acinetobacter, Penicillium, and Aspergillus fumigatus were cultured from nasal secretions (father and daughter). RT-PCR revealed A. fumigatus DNA in sinus tissues of the daughter. The dog had 72 skin lesions (sebaceous glands and lipomas) from which trichothecenes and ochratoxin A. were detected. The health of the family is discussed in relation to the most recent published literature regarding microbial contamination and toxic by-products present in water-damaged buildings.

Chronic sinusitis: defective T-cells responding to superantigens, treated by reduction of fungi in the nose and air.

In this study, the author used endoscopic sinus photography to study the effects of reduction of fungi in the nose, and in environmental air, on the sinus mucosa of 639 patients diagnosed with chronic rhinosinusitis. Sinus mucosal photographs were taken before and after reduction of fungal load in the nose and air, to determine if there was an optimum environmental air fungal load associated with sinus mucosal recovery to normal appearance. Systemic symptoms associated with fungal exposure, which resolved when fungus was removed from the patient and the environmental air and reappeared with recurrent environmental fungal exposure, are also discussed and are termed systemic fungal symptoms. Interventions consisted of nasal fungal load reduction with normal saline nasal irrigations and antimicrobial nasal sprays, and environmental air fungal load reduction with high-efficiency particulate air (HEPA) filtration in combination with ionizers or evaporation of a solution of botanical extract. Main outcome measures were obtained with environmental air 1-hr gravity-plate fungal colony counts, laser air particle counts, and endoscopic sinus photography. Blood levels of immunoglobulins IgG and IgE for 7 common molds were also determined. After intervention, 94% of patients who used antimicrobial nasal sprays and who reduced their environmental fungal air count to 0-4 colonies per 1-hr agar gravity-plate exposure (n = 365) exhibited normal sinus mucosa by endoscopic exam. Environmental air fungal counts that exceeded 4 colonies resulted in sinus mucosal abnormalities ranging from edema, to pus and/or nasal polyps at higher counts. Neutralization of allergy, and/or surgery, were used as appropriate following implementation of environmental measures. On the basis of these observations, as well as detailed clinical experience and a review of the current literature, the author hypothesizes that the pathogenesis of chronic rhinosinusitis, allergic fungal sinusitis, and systemic fungal symptoms is a genetic defect at the variable beta chain helper T-cell receptor (TCR Vbeta) site which requires the presence of an antigen (fungus). Chronic sinusitis patients who have recurring exposure to environmental air that contains fungal concentrations in excess of 4 colonies per 1-hr agar plate exposure appear to have an increased risk of persistent chronic sinusitis and/or systemic symptoms, regardless of the medical treatment provided.